What is the most likely diagnosis?A 35-year-old woman with a history of asthma presents to your office with symptoms of nasal itching, sneezing, and rhinorrhea. She states she feels this way most days but her symptoms are worse in the spring and fall. She has had difficulty sleeping because she is always congested. She states she has taken diphenhydramine (Benadryl) with no relief. She does not smoke cigarettes and does not have exposure to passive smoke but she does have two cats at home. On examination, she appears tired but is in no respiratory distress. Her vital signs are temperature, 98.8°F; blood pressure, 128/84 mm Hg; pulse, 88 beats/min; and respiratory rate, 18 breaths/min. The mucosa of her nasal turbinates appear swollen (boggy) and have a pale, bluish-gray color. Thin and watery secretions are seen. No abnormalities are seen on ear examination. There is no cervical lymphadenopathy noted and her lungs are clear.
What is the most likely diagnosis?
What is your next step?
What are important considerations and potential complications of management?
Summary: A 35-year-old asthmatic woman complains of chronic nasal congestion that is worse in the spring and the fall.
• Most likely diagnosis: Allergic rhinitis.
• Next step in management of this patient: Treatment with antihistamines, decongestants, or intranasal steroids. These treatments can also be used in combination with each other.
• Considerations and possible complications of therapy: Recognition and reduction of potential allergen exposure will yield more success in management than pharmacotherapy alone. Excessive use of topical decongestants can cause rebound congestion.
1. Understand the inflammatory nature of allergic rhinitis.
2. Recognize physical examination findings consistent with allergic rhinitis.
3. Develop an approach to the management of allergic rhinitis, including the roles of pharmacotherapy and reduction of allergen exposure.
4. Recognition and management of asthma.
5. Identification of essential features and treatment of anaphylaxis.
This patient presents with a classic history of allergic rhinitis. Her history of itchy eyes, nasal congestion and discharge, and seasonal in nature (worse in spring and fall) are all consistent with allergic rhinitis. Her examinations are also consistent with the diagnosis. The mucosa of her nasal turbinates appear swollen (boggy) and have a pale, bluish-gray color. Thin and watery secretions are seen. The best therapy for this condition is avoidance of allergens, but due to the probable allergy to pollen, this can be very difficult. Nasal corticosteroids offer the most consistent symptomatic relief.
ALLERGIC RHINITIS: Inflammation of the nasal passages caused by allergic reaction to airborne substances.
ANAPHYLAXIS: Rapidly progressing, life-threatening allergic reaction, mediated by immunoglobulin E (IgE) immediate hypersensitivity reaction.
Rhinitis is inflammation of the nasal membranes and is characterized by any combination of the following: sneezing, nasal congestion, nasal itching, and rhinorrhea. The eyes, ears, sinuses, and throat can also be involved. Allergic rhinitis is the most common cause of rhinitis, occurring in up to 20% of the population.
Allergic rhinitis involves inflammation of the mucous membranes of the nose, eyes, eustachian tubes, middle ear, sinuses, and pharynx. Inflammation of the mucous membranes is characterized by a complex interaction of inflammatory mediators but, ultimately, is triggered by an IgE-mediated response to an extrinsic protein.
In susceptible individuals, exposure to certain foreign proteins leads to allergic sensitization, which is characterized by the production of specific IgE directed against these proteins. This specific IgE coats the surface of mast cells, which are present in the nasal mucosa. When the specific allergen is inhaled into the nose, it can bind to the IgE in the mast cells, leading to the delayed release of a number of mediators.
Mediators that are immediately released include histamine, tryptase, chymase, and kinase. Mast cells quickly synthesize other mediators, including leukotrienes and prostaglandin D2. Symptoms can occur quickly after exposure. Mucous glands are stimulated, leading to increased secretions. Vasodilation occurs, causing congestion. Stimulation of sensory nerves leads to sneezing and itching. Other symptoms include the redness and tearing of eyes, postnasal drip, and ear pressure.
Over the next 4 to 8 hours, these mediators, through a complex interplay of events, recruit neutrophils, eosinophils, lymphocytes, and macrophages to the mucosa. These inflammatory cells cause more congestion and mucus production that may persist for hours or days. Systemic effects, including fatigue, sleepiness, and malaise, can result from the inflammatory response as well.
Obtaining a detailed history is important in the evaluation of allergic rhinitis, as specific triggers may be identified. Evaluation should include the nature, duration, and time course of symptoms. The recent use of medications is another important consideration as are a family history of allergic diseases, environmental exposures, and comorbid conditions.
Part of the history should include the time pattern of symptoms and whether symptoms occur at a consistent level throughout the year (perennial rhinitis), only occur in specific seasons (seasonal rhinitis), a combination of the two, or in relation to a workplace (occupational rhinitis). Trigger factors such as exposure to pollens, mold spores, specific animals, or cleaning of the house can sometimes be identified. Irritant triggers such as smoke, pollution, and strong smells can aggravate symptoms of allergic rhinitis. Response to treatment with antihistamines supports the diagnosis of allergic rhinitis.
Symptoms that can be associated with allergic rhinitis include sneezing, itching (of nose, eyes, or ears), rhinorrhea, postnasal drip, congestion, anosmia, headache, earache, tearing, red eyes, and drowsiness.
Common findings on examination include “allergic shiners,” which are dark circles around the eyes related to vasodilation or nasal congestion. The “nasal crease” can be seen in some cases. It is a horizontal crease across the lower half of the bridge of the nose caused by repeated upward rubbing of the tip of the nose by the palm of the hand (“allergic salute”).
Examination of the nose may reveal mucosa of the nasal turbinates to be swollen (boggy) and have a pale, bluish-gray color. Assessment of the character and quantity of nasal mucus may be helpful in ascertaining a diagnosis. Thin and watery secretions are frequently associated with allergic rhinitis, whereas thick and purulent secretions are usually associated with sinusitis. The characteristic of the mucous is not always diagnostic, as thick, purulent, colored mucus can also occur with allergic rhinitis.
The nasal cavity should be inspected for growths such as polyps or tumors. Polyps are firm, gray masses that are often attached by a stalk, which may not be visible. After spraying a topical decongestant, polyps do not shrink, whereas the surrounding nasal mucosa does shrink. Examine the nasal septum to look for any deviation or septal perforation that may be present as a consequence of chronic rhinitis, granulomatous disease, cocaine abuse, prior surgery, topical decongestant abuse, or, rarely, topical steroid overuse.
Otoscopy should be performed to look for tympanic membrane retraction, air-fluid levels, or bubbles. Performing pneumatic otoscopy can be considered to look for abnormal tympanic membrane mobility. These findings can be associated with allergic rhinitis, particularly if eustachian tube dysfunction or secondary otitis media is present. Ocular examination may reveal findings of injection and swelling of the palpebral conjunctivae, with excess tear production. Dennie-Morgan lines (prominent creases below the inferior eyelid) are associated with allergic rhinitis.
“Cobblestoning” of the posterior pharynx is often observed. This is caused by the presence of streaks of lymphoid tissue on the posterior pharynx. Tonsillar hypertrophy can also be seen. The neck should be examined for the presence of lymph-adenopathy. The respiratory system must be examined for findings consistent with asthma. These include wheezing, tachypnea, and a prolonged expiratory phase of respiration.
The causes of allergic rhinitis can differ depending on whether the symptoms are seasonal, perennial, or sporadic/episodic. Some patients are sensitive to multiple allergens and can have perennial allergic rhinitis with seasonal exacerbations. Although food allergy can cause rhinitis, particularly in children, it is rarely a cause of allergic rhinitis in the absence of gastrointestinal or skin symptoms. Seasonal allergic rhinitis is commonly caused by allergy to seasonal pollens and outdoor molds.
Tree pollens, which vary by geographic location, are typically present in high counts during the spring, although some species produce their pollens in the fall. Grass pollens also vary by geographic location. Most of the common grass species are associated with allergic rhinitis. A number of these grasses are cross-reactive, meaning that they have similar antigenic structures (ie, proteins recognized by specific IgE in allergic sensitization). Consequently, a person who is allergic to one species is also likely to be sensitive to a number of other species. The grass pollens are most prominent from the late spring through the fall, but can be present year-round in warmer climates.
Weed pollens also vary geographically. Many weeds, such as short ragweed, a common cause of allergic rhinitis in much of the United States, are most prominent in the late summer and fall. Other weed pollens are present year-round, particularly in warmer climates.
Perennial allergic rhinitis is typically caused by allergens within the home, but can also be caused by outdoor allergens that are present year-round. In warmer climates, grass pollens can be present throughout the year. In some climates, individuals may be symptomatic because of trees and grasses in the warmer months and molds and weeds in the winter.
In the United States, two major house dust mite species are associated with allergic rhinitis. These mites feed on organic material in households, particularly the skin that is shed from humans and pets. They can be found in carpets, upholstered furniture, pillows, mattresses, comforters, and stuffed toys. Exposure can be reduced by methods such as carpet removal; however, current studies have not found any benefit to using mite-proof mattresses or pillow covers.
Allergy to indoor pets is a common cause of perennial allergic rhinitis. Cat and dog allergies are encountered most commonly in clinical practice. However, allergies have been reported to occur with most of the furry animals and birds that are kept as indoor pets. Although cockroach allergy is most frequently considered to be a cause of asthma, particularly in the inner city, it can also cause perennial allergic rhinitis in infested households. Rodent infestation may also be associated with allergic sensitization.
The management of allergic rhinitis consists of four major categories of treatment: patient education, allergen avoidance, pharmacologic management, and immuno-therapy. All aspects of treatment are more successful when exposure to allergens is decreased.
Recommendations for treatment are primarily based on symptoms and patient age. Pharmacotherapy can involve the use of antihistamines, decongestants, intra-nasal corticosteroids, and, in severe cases, systemic corticosteroids. Antihista-mines competitively antagonize the receptors for histamine, which is released from mast cells. This reduces the production of symptoms mediated by the release of histamine. “First-generation” antihistamines including diphenhydramine, chlorpheniramine, and hydroxyzine are inexpensive and available over the counter. Side effects include sedation and the anticholinergic effects of dry mouth, dry eyes, blurred vision, and urinary retention; therefore, their use should be monitored in sensitive populations, such as the elderly. Newer, so-called second-generation antihistamines, including loratadine, desloratadine, fexofenadine, and cetirizine, have much less penetration into the central nervous system, resulting in a lower incidence of sedation as a side effect (except for cetirizine). They also have fewer anticholinergic effects. They are, however, significantly more expensive than the older agents. Loratadine, fexofenadine and cetirizine have recently become available without a prescription. Oral antihistamines begin to take effect within 15 to 30 minutes after ingestion and are best used in persons with mild and intermittent symptoms.
Decongestants, either given orally or intranasally, can be used to provide symptomatic relief of nasal congestion. These agents constrict blood vessels in the nasal mucosa and reduce the overall volume of the mucosa. The most commonly used agent is pseudoephedrine, an α-adrenoreceptor agonist. Oral decongestants can cause tachycardia, tremors, and insomnia. Rebound hyperemia and worsening of symptoms can occur with chronic use or upon discontinuation of nasal decongestants.
Corticosteroid nasal sprays are the most effective treatment and first-line therapy for the long-term management of mild to moderate persistent symptoms of allergic rhinitis. They reduce the production of inflammatory mediators and the recruitment of inflammatory cells. Systemic absorption of the steroid is relatively low, reducing the risk of complications associated with the chronic use of systemic corticosteroids. Side effects include nosebleeds, pharyngitis, and upper respiratory tract infections. Maximal effectiveness is achieved after 2 to 4 weeks of use.
Leukotriene inhibitors (zafirlukast, montelukast, zileuton) are indicated both for allergic rhinitis and for maintenance therapy for persistent asthma. They are particularly useful in patients with both asthma and allergies or in those whose asthma may be triggered by allergens. Although useful, they have not been proven to be superior to corticosteroid nasal sprays alone. Leukotriene inhibitors are taken orally and are only available by prescription.
Oral corticosteroids are potent inhibitors of cell-mediated immunity. The use of systemic steroids is limited by adverse effects, including suppression of the hypothalamic-pituitary-adrenal axis and hyperglycemia. Long-term use can lead to peptic ulcer formation, increased susceptibility to infection, poor wound healing, and the reduction of bone density. Because of these significant risks, systemic steroids are used only for severe allergies and are used in the lowest effective dose for the shortest possible time.
Desensitization therapy is frequently attempted in patients who remain symptomatic despite maximal medical therapy. The first step of this treatment is to test for specific antigens to which the person is allergic. The second step is to inject the patient with highly diluted concentrations of this antigen. The concentration of the antigen(s) in the injection is gradually increased, in an effort to reduce the patient’s inflammatory response to the antigen(s). Injections are typically given weekly or biweekly. This process is expensive, time-consuming, and requires numerous injections. Patients and physicians must be prepared to address severe, even anaphylactic, reactions that may occur during the process.
Urticaria is characterized by large, irregularly shaped, pruritic, erythematous wheals. Angioedema is painless, deep, subcutaneous swelling that often involves the periorbital, circumoral, and facial regions. Anaphylaxis is a systemic reaction with cutaneous symptoms that is associated with dyspnea, visceral edema, and hypotension. The manifestations of anaphylaxis include hypotension or shock from widespread vaso-dilation, respiratory distress from bronchospasm or laryngeal edema, gastrointestinal and uterine muscle contraction, and urticaria and angioedema.
At the first suspicion of anaphylaxis, aqueous epinephrine 1:1000, in a dose of 0.2 to 0.5 mL (0.2-0.5 mg) is injected subcutaneously or intramuscularly. Repeated injections can be given every 15 to 30 minutes when necessary. Rapid intravenous infusion of large volumes of fluids (saline, lactated Ringer solution, plasma or plasma expanders) is essential to replace loss of intravascular plasma into tissues. Airway obstruction may be caused by edema of the larynx or by bronchospasm. Endotracheal intubation may be required. Bronchospasm responds to subcutaneous epinephrine or terbutaline. Antihistamines may be useful as adjuvant therapy for alleviating cutaneous manifestations of urticaria or angioedema and pruritus. All patients with anaphylaxis should be monitored for a period of time, for example, 24 hours.
Conjunctivitis is an infection of the palpebral and/or bulbar conjunctiva. It is the most common eye disease seen in community medicine. Most cases are caused by bacterial or viral infection. Other causes include allergy and chemical irritants. The mode of transmission of infectious conjunctivitis is usually direct contact to the opposite eye or to other persons via fingers, towels, or handkerchiefs.
The organisms isolated most commonly in bacterial conjunctivitis are Staphylococcus, Streptococcus, Haemophilus, Moraxella, and Pseudomonas. There is no blurring of vision and only mild discomfort. In severe cases, examination of stained conjunctival scrapings and cultures are recommended. The disease is usually self-limited, lasting about 10 to 14 days if untreated. A sulfonamide instilled locally three times daily will usually clear the infection in 2 to 3 days.
Epidemic keratoconjunctivitis (pink eye) is highly contagious and spread by person-to-person contact or fomites. The most common cause is adenovirus. It is usually associated with pharyngitis, fever, malaise, and preauricular lymphadenopathy. Locally, the palpebral conjunctiva is red with a copious watery discharge and scanty exudates. Local sulfonamide therapy might prevent secondary bacterial infection; hot compresses reduce the discomfort of the associated lid edema; weak topical steroids may be necessary to treat the corneal infiltrates. The disease usually lasts at least 2 weeks.
Noninfectious causes of conjunctivitis include allergic and chemical irritants. Symptoms of allergic conjunctivitis include itching, tearing, redness, stringy discharge, and sometimes photophobia. Treatment can include the use of oral antihistamines or topical antihistamine or anti-inflammatory eye drops.
6.1 A 30-year-old man has both mild persistent asthma and chronic environmental allergies. Which of the following medications is indicated for the management of this patient’s conditions?
A. Inhaled albuterol (short-acting β-adrenergic agonist)
B. Intranasal fluticasone (corticosteroid)
C. Oral montelukast (leukotriene modifier)
D. Oral cetirizine (second-generation antihistamine)
6.2 A 12-year-old adolescent male presents with eye itching and redness. He has clear drainage from his eyes but no crusting. Examination today is normal except for mildly injected conjunctiva bilaterally. Which of the following is the most appropriate treatment?
A. Antibiotic eye drops
B. Ophthalmology consultation
C. Anti-inflammatory eye drops
D. Oral leukotriene inhibitor
6.3 A 56-year-old man presents to his physician with symptoms consistent with allergic rhinitis. His past medical history is positive for benign prostatic hyper-plasia. He continues to work in a warehouse as a forklift operator. Which of the following medications should be used to treat this patient?
A. Diphenhydramine
B. Hydroxyzine
C. Chlorpheniramine
D. Fexofenadine
6.1 C. Montelukast is indicated for both the management of persistent asthma and chronic allergies. Nasal steroids and oral antihistamines are indicated only for allergies.
6.2 C. This patient has allergic conjunctivitis. Topical anti-inflammatory drops are appropriate therapy. Other options would include topical or oral antihistamines. The other therapies listed are not appropriate in this condition.
6.3 D. The second-generation antihistamines, such as fexofenadine, are less sedating and have fewer anticholinergic side effects than the first-generation anti-histamines. They would be a better choice for someone who operates heavy machinery and has benign prostatic hyperplasia. However, they are no more effective at symptom relief than the first-generation antihistamines listed above.
The management of allergic rhinitis consists of four major categories of treatment: patient education, allergen avoidance, pharmacologic management, and immunotherapy.
At the first suspicion of anaphylaxis, aqueous epinephrine 1:1000 in a dose of 0.2 to 0.5 mL (0.2-0.5 mg) is injected subcutaneously or intramuscularly. The airway should always be assessed and patient intubated if necessary to secure breathing.
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